BMI, BMR & TDEE Calculator Body Composition and Daily Energy Needs

What this calculator actually does

This page does three things, and it does them separately. It works out your body mass index, which is a rough measure of whether your weight is proportionate to your height. It works out your basal metabolic rate, which is roughly how many calories your body would burn in a day if you did nothing but rest. And it works out your total daily energy expenditure, which is your basal rate adjusted for how active you actually are.

Each of those numbers answers a slightly different question. BMI answers "roughly where does my weight sit for my height?" BMR answers "how much energy do I burn just existing?" TDEE answers "how much energy do I burn on a real day, given the way I live?" Used together, they give you a clearer picture than any one of them alone.

Every calculation runs inside your browser. When you press Calculate, the maths happens on your device using the numbers you typed. The result appears on your screen and disappears the moment you close the tab. The one exception is the optional AI insight button further up this page. That button sends a short, anonymous summary of your result to a small serverless function only when you press it, and only to generate a short written explanation. If you never press it, nothing about your calculation leaves your device at all.

What BMI measures, and what it does not

Body mass index is the relationship between your weight and your height. You take your weight in kilograms, divide it by the square of your height in metres, and you have your BMI. That is the entire formula. It was first proposed in the 1830s by a Belgian statistician named Adolphe Quetelet, who was trying to describe populations rather than individuals. That origin still matters, because it explains what BMI is good at and where it goes wrong.

At a population level, BMI is genuinely useful. Across millions of people, there is a consistent statistical relationship between a higher BMI and a higher risk of conditions like type 2 diabetes, high blood pressure, heart disease, and joint problems. Public health agencies rely on it because it is fast, cheap, and reasonably predictive when applied broadly.

At an individual level, though, BMI has real blind spots. It cannot tell the difference between muscle and fat. It cannot tell where on your body your weight sits, which matters a lot because fat around the abdomen carries far more metabolic risk than fat around the hips and thighs. It cannot tell whether your weight has changed because you gained muscle or lost it. It is, in short, a broad screening tool, not a full assessment.

A rugby player at the top of his game, weighing 105 kilograms at 1.85 metres, will calculate a BMI of 30.7 and be classified as obese by the standard thresholds. He is not obese. His body composition is dominated by muscle. A similar number can show up for someone with very little muscle and a lot of visceral fat, whose risk profile is completely different. BMI sees neither of them clearly.

The WHO BMI categories

The World Health Organization publishes the categories most countries use. They were designed for adults aged twenty and older. Here is the full table, along with the clinical meaning of each band.

Two caveats apply to this table. First, the WHO itself recommends lower thresholds for people of South Asian, East Asian, and some African ancestries, because the same BMI tends to correspond to more body fat and more metabolic risk in those populations. Under the adjusted thresholds, overweight begins at 23.0 and obesity at 27.5. Second, the table does not apply to children, teenagers, pregnant women, or highly muscular athletes. Each of those groups needs different reference points.

BMI Prime in plain terms

BMI Prime is an alternative way of reading the same number. Instead of expressing your BMI on its own, you divide it by 25, which is the upper edge of the healthy range. The result tells you how far you are from that edge as a proportion.

A BMI Prime of 0.85 means you are at 85 percent of the healthy ceiling. A BMI Prime of 1.00 means you are exactly at the boundary between healthy and overweight. A BMI Prime of 1.20 means you are twenty percent above the healthy ceiling. A BMI Prime of 0.72 means you are twenty-eight percent below it, and therefore underweight.

The reason some clinicians prefer BMI Prime is that it makes the comparison to the healthy limit more intuitive. If your BMI is 27.5, the number alone does not tell you much. If your BMI Prime is 1.10, you immediately know you are ten percent above the healthy limit. That framing can be easier to work with when you are setting a target.

Why BMI is only a starting point

If BMI is this limited, why does anyone use it? Because it is a fast, universally available first filter. A doctor with ten minutes and no equipment can take your height and weight and get a number that flags whether a deeper conversation is needed. That is genuinely useful. The mistake is treating that first filter as the final answer.

Three tools fill in the picture that BMI misses.

Waist circumference is the simplest. Measure around your belly button with a tape measure, without pulling it tight. For most adults, risk rises when the waist goes above 94 centimetres (37 inches) for men and 80 centimetres (31.5 inches) for women. Above 102 centimetres (40 inches) for men and 88 centimetres (35 inches) for women, the risk is substantially higher.

Waist-to-height ratio is even simpler. Divide your waist measurement by your height. If the answer is below 0.5, you are in a good place. If it is above 0.5, you are carrying more abdominal fat than is ideal, regardless of what your BMI says. This single ratio is one of the strongest predictors of cardiometabolic risk available without laboratory testing.

Body fat percentage gives you the most detail, but it is harder to measure accurately outside a clinic. The most accurate methods involve equipment that most people do not have access to. Consumer scales and handheld devices give numbers that vary widely from one device to the next. A rough estimate is usually enough for tracking your own progress over time, as long as you use the same method each time and do not treat the exact figure as gospel.

BMR and the Mifflin-St Jeor equation

Your basal metabolic rate is the amount of energy your body uses to keep you alive while you are at complete rest. Your heart is beating, your lungs are breathing, your kidneys are filtering, your brain is running, your cells are repairing themselves. All of that costs energy, and BMR is the measure of that cost over twenty-four hours.

For most people, BMR accounts for sixty to seventy-five percent of everything you burn in a day. That is why it matters so much: even a modest change to your baseline metabolism has a bigger effect on your daily energy budget than an extra hour at the gym.

The equation this calculator uses is called the Mifflin-St Jeor equation, and it was published in 1990 in the American Journal of Clinical Nutrition. It is the most widely used modern predictive formula because a large body of research has shown it to be more accurate than the older Harris-Benedict equations for most people. Here is the formula itself.

For men: BMR = (10 × weight in kilograms) + (6.25 × height in centimetres) − (5 × age in years) + 5

For women: BMR = (10 × weight in kilograms) + (6.25 × height in centimetres) − (5 × age in years) − 161

Notice that the only difference between the two is the final constant: plus five for men, minus one hundred and sixty-one for women. This reflects the average difference in lean body mass and hormonal profile between the two groups. It is an average, not a rule, which is one reason the number you get is an estimate rather than a precise reading.

To see it in action, take a thirty-five year old man weighing 80 kilograms at 180 centimetres. His BMR is (10 × 80) + (6.25 × 180) − (5 × 35) + 5, which equals 800 + 1,125 − 175 + 5, for a total of 1,755 calories per day. If you fed him exactly that many calories and he truly did nothing but rest, his weight would stay roughly steady.

TDEE and activity levels

Nobody actually rests all day. You walk to the bathroom, you make food, you sit at a desk, you stand in a queue, you carry shopping, you play with your children, you go for a run. All of that adds to your energy expenditure, and the combined total is what we call your total daily energy expenditure, or TDEE.

To estimate TDEE, the calculator multiplies your BMR by an activity multiplier. The five options on the form correspond to the five standard multipliers used in nutrition research.

• Sedentary (1.20): A desk job, minimal walking, no structured exercise. This is the correct choice for most people who work in offices or at computers and do not exercise deliberately.
• Lightly active (1.375): Light exercise one to three days a week, or a job that involves some walking, such as teaching or retail.
• Moderately active (1.55): Moderate exercise three to five days a week, or a fairly physical job combined with light training.
• Very active (1.725): Hard training six or seven days a week, or a physically demanding job combined with regular exercise.
• Extra active (1.90): A very physical job such as construction, combined with twice-daily training, or full-time athletic preparation.

The single most common mistake people make with these calculators is picking a multiplier that flatters them. Studies that compared self-reported activity to measured activity consistently find that most people overestimate how much they move. If you work a desk job, exercise three times a week for an hour, and walk a bit on weekends, you are probably in the lightly active bracket, not the very active one. Choosing the higher number does not make your body burn more calories. It just makes your estimate wrong.

Turning numbers into a daily calorie target

Once you have a TDEE, you have a reference point. That figure is roughly the number of calories you would need to eat each day to stay at the same weight. From there, the adjustments are simple arithmetic.

To lose fat, subtract somewhere between 250 and 500 calories. The smaller figure produces slower but more comfortable progress, usually around a quarter of a kilogram per week. The larger figure produces about half a kilogram per week, which is the rate most guidelines consider safe and sustainable. Bigger deficits than that tend to produce faster loss at first, then rebound as your metabolism adjusts and hunger becomes difficult to manage.

To gain muscle, add about 250 calories. This small surplus is enough to support muscle protein synthesis during resistance training without adding unnecessary fat. Larger surpluses tend to add fat more efficiently than they add muscle, unless you are a complete beginner or are training under professional supervision.

The important thing is that these targets are starting points. Your real TDEE will be somewhere close to the estimate, but the exact number can be off by one or two hundred calories. The way to find your true maintenance level is to eat at your estimated TDEE for two to three weeks, weigh yourself at the same time each morning, and adjust based on what actually happens. If your weight stays flat, the estimate was accurate. If it drifts up or down, your real maintenance sits slightly below or above the estimate, and you can correct accordingly.

Common mistakes when using these numbers

A few pitfalls show up again and again when people start working with BMI, BMR, and TDEE.

Treating BMI as a diagnosis. It is a screening tool. A BMI of 27 does not mean you have a health problem. It means your weight-for-height ratio sits in a band that is worth a closer look, which is exactly what the calculator is designed to prompt.

Overestimating activity. Already covered above, but it is the single most common source of error. When in doubt, pick the lower multiplier. You can always adjust after seeing what happens on the scale.

Chasing the exact number. If your TDEE comes out as 2,347 calories and another calculator says 2,312, that difference is meaningless. Both are estimates with a margin of error of a couple hundred calories. Work in round numbers and adjust based on results, not on decimal places.

Eating back every calorie you burn. Fitness trackers tend to overestimate calories burned during exercise, sometimes by a wide margin. If you eat back everything your watch claims you burned, you will often end up eating more than your actual TDEE.

Ignoring the scale for too long. Body weight fluctuates day to day because of water, salt, hormones, and food in transit. That is why you weigh yourself at the same time every morning and look at the weekly trend rather than any single reading. It is also why a two or three week window is the shortest useful timeframe for judging whether a calorie target is working.

When to see a professional

Numbers from a calculator can be useful for personal planning, but they cannot replace the judgement of a trained clinician. There are specific situations where that judgement matters enough to seek it out.

If your BMI sits below 17 or above 35, a medical review is worth arranging regardless of how you feel. Both extremes carry risks that are better addressed early. If you have lost or gained a significant amount of weight without meaning to, that is another signal that a doctor should take a look. If you have an existing condition such as diabetes, thyroid disease, kidney disease, or an eating disorder, any calorie target should be set with your treating professional rather than from a website. And if you are pregnant or breastfeeding, your energy needs are completely different from the standard formulas here.

For everyone else, the numbers on this page are a reasonable starting point for personal planning. Bring them to a professional if you want a fuller picture, and treat them as one input among many rather than the final word on your health.

Ethnic and regional nuances: why universal cutoffs mislead

The standard WHO Body Mass Index classification thresholds (18.5 for underweight, 25.0 for overweight, and 30.0 for obesity) were primarily established using epidemiologic data collected from populations of European descent. However, extensive clinical research over the past two decades has established that the relationship between BMI, percentage body fat, and cardiometabolic morbidity differs dramatically across global ethnicities and ancestry backgrounds.

For individuals of South Asian, East Asian, and Southeast Asian descent, the risk of developing type 2 diabetes mellitus, systemic hypertension, atherogenic dyslipidemia, and premature cardiovascular disease rises at substantially lower BMI values than in Western populations. A landmark WHO expert consultation acknowledged this divergence, establishing provisional lowered action triggers for Asian populations:

The pathophysiological reason for this lowered threshold lies in body composition phenotype. South Asian individuals tend to possess a higher percentage of body fat at any given BMI compared to Caucasian equivalents, a clinical phenotype frequently described as the "thin-fat" or "metabolically obese normal-weight" phenomenon. They exhibit a pronounced tendency toward ectopic lipid deposition in visceral compartments, skeletal muscle, and hepatic tissue, alongside reduced skeletal muscle mass and lower capacity for peripheral glucose disposal. Consequently, an individual of Indian or Pakistani descent with a BMI of 23.5 kg/m² may exhibit the metabolic inflammation and insulin resistance typical of a European individual with a BMI of 27.0 kg/m².

Conversely, populations of African, Polynesian, and Māori heritage often demonstrate greater bone mineral density and higher proportions of appendicular lean muscle mass per unit of height. For these groups, standard BMI formulas frequently overestimate actual body adiposity, classifying lean, muscular individuals as overweight. These pronounced population differences emphasize why clinical bodies such as the UK National Institute for Health and Care Excellence (NICE) explicitly mandate lowered trigger thresholds (23.0 kg/m² for overweight, 27.5 kg/m² for obesity) when assessing individuals of Black, Asian, and other minority ethnic backgrounds.

Visceral vs. subcutaneous fat: the clinical power of WHtR and WHR

Adipose tissue is not a uniform, inert storage depot. From a pathophysiological standpoint, fat behaves as an active, heterogeneous endocrine organ, and its anatomical distribution determines its risk profile far more decisively than its total aggregate mass.

Clinicians divide body fat into two primary compartments:

• Subcutaneous Adipose Tissue (SAT): Located directly beneath the dermis, particularly around the hips, thighs, and lower abdomen. Subcutaneous fat functions predominantly as mechanical cushioning, thermal insulation, and an energy buffer. While excessive SAT contributes to joint stress and mobility challenges, it is metabolically benign compared to visceral fat and exhibits higher responsiveness to insulin and greater leptin secretion.
• Visceral Adipose Tissue (VAT): Packed deep within the peritoneal cavity surrounding vital mesenteric organs including the liver, pancreas, intestines, and kidneys. Visceral fat cells have high lipolytic activity and resist insulin. Crucially, blood draining from visceral fat enters the portal venous circulation directly into the liver. This portal flux floods hepatocytes with non-esterified free fatty acids, triggering hepatic insulin resistance, impaired clearance of hepatic glucose, increased very-low-density lipoprotein (VLDL) synthesis, and systemic atherogenic dyslipidemia.

Visceral adipocytes are also heavily infiltrated by pro-inflammatory M1-polarized macrophages. These cells secrete elevated levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and plasminogen activator inhibitor-1 (PAI-1), while downregulating the cardioprotective peptide adiponectin. This chronic, subclinical inflammatory cascade accelerates endothelial dysfunction, promotes plaque instability, and quadruples the risk of non-alcoholic fatty liver disease (now termed metabolic dysfunction-associated steatotic liver disease, or MASLD).

Because standard BMI cannot differentiate between protective subcutaneous fat and toxic visceral fat, two simple tape-measure indexes provide indispensable clinical refinement:

1. Waist-to-Height Ratio (WHtR): A universal, sex-agnostic metric summarized by the clinical rule: "Keep your waist circumference to less than half your height." Extensive systematic reviews and meta-analyses published in the British Medical Journal and Obesity Reviews confirm that a WHtR of 0.50 or higher serves as a superior predictor of all-cause mortality, cardiovascular events, and type 2 diabetes than BMI alone.

2. Waist-to-Hip Ratio (WHR): Reflects central "android" (apple-shaped) versus peripheral "gynoid" (pear-shaped) fat distribution. The World Health Organization defines substantially elevated metabolic risk as a WHR above 0.90 for men and above 0.85 for women.

Metabolic paradoxes: normal weight obesity and sarcopenic obesity

Relying exclusively on bathroom scale numbers creates two dangerous clinical blind spots that affect millions of unsuspecting individuals: Normal Weight Obesity and Sarcopenic Obesity.

Normal Weight Obesity (NWO), popularly described as being "metabolically obese normal-weight" or "skinny-fat," describes individuals whose BMI falls comfortably within the conventional normal bracket (18.5 – 24.9 kg/m²), but whose percentage of body fat exceeds clinical safety standards—typically defined as greater than 30% in biological women and greater than 23% in biological men. These individuals appear slender in everyday clothing and frequently pass routine workplace screenings with a "clean" health bill based on BMI alone.

Beneath the surface, however, individuals with NWO exhibit a constellation of metabolic derangements virtually identical to individuals with clinical obesity: elevated fasting insulin, atherogenic small-dense low-density lipoprotein (sdLDL) particles, elevated high-sensitivity C-reactive protein (hs-CRP), subclinical vascular stiffness, and hepatic steatosis. Because their low overall body weight is driven by inadequate skeletal muscle mass rather than low body fat, their basal glucose disposal capacity is severely compromised, placing them at fivefold higher risk for premature metabolic syndrome compared to metabolically healthy lean peers.

The companion condition is Sarcopenic Obesity, which predominantly threatens aging adults and chronically sedentary individuals. Sarcopenia is the age-related involuntary loss of skeletal muscle mass, quality, and contractile force. As adults age without consistent resistance exercise stimulus, they lose roughly 3% to 8% of their muscle mass per decade after age 30, with the rate accelerating after age 60.

When muscle loss occurs concurrently with creeping fat accumulation, the bathroom scale creates a dangerous optical illusion: an older adult may weigh exactly 72 kilograms at age 40 and still weigh 72 kilograms at age 68. Their BMI registers as unchanged. However, their internal composition has shifted catastrophically: eight kilograms of metabolically active contractile skeletal muscle have vanished, replaced by eight kilograms of visceral and intramuscular adipose tissue. This silent transition degrades functional autonomy, impairs mitochondrial density, worsens balance and fall risk, and severely hampers systemic glycemic control.

The Quetelet scaling limitation & the Oxford Trefethen formula

To understand why BMI sometimes yields bizarre classifications, one must examine the 19th-century mathematical history of the formula itself. Belgian astronomer, mathematician, and statistician Adolphe Quetelet introduced the ratio of mass to height squared in 1832. Quetelet was not a medical doctor; he was developing the concept of "l'homme moyen" (the average man) to study population statistics for social sciences.

From a purely geometric perspective, human beings are three-dimensional physical entities. If a human body were to scale uniformly and isometrically across all three spatial axes (height, width, and depth), their volume and mass would increase proportionately with the cube of height (height³). Quetelet observed that human growth is not strictly isometric; taller humans are proportionately slightly more slender than shorter humans. He concluded that squaring height (height²) provided a convenient mathematical compromise for 19th-century European population statistics.

However, this mathematical compromise introduces systematic distortion at the height extremes:

• Distortion for tall individuals: Standard BMI divides weight by height squared, failing to account for the full volumetric expansion of taller frames. As a result, standard BMI systematically inflates numbers for tall individuals, frequently labeling tall, lean people as overweight or obese.
• Distortion for short individuals: Standard BMI divides by too small a denominator for shorter statures, underestimating actual adiposity and giving shorter individuals with high body fat a falsely reassuring "normal" score.

In 2013, Professor Nick Trefethen, head of Numerical Analysis at the University of Oxford, proposed an empirically refined equation that corrects this volumetric scaling flaw:

Oxford BMI Formula (Metric): BMI = 1.3 × Weight (kg) ÷ [Height (m)]^2.5

Oxford BMI Formula (Imperial): BMI = 5734 × Weight (lbs) ÷ [Height (in)]^2.5

For an individual of average height (around 168 cm or 5'6"), both formulas yield virtually identical numbers. But for a tall individual measuring 198 cm (6'6") weighing 95 kg, standard BMI yields 24.2 kg/m², whereas the Oxford formula yields 22.8 kg/m²—a difference of nearly 1.5 full BMI points. For individuals seeking a true athletic benchmark, sports scientists also compute the Fat-Free Mass Index (FFMI):

FFMI = Lean Mass (kg) ÷ [Height (m)]^2

FFMI isolates skeletal muscle, bone, and organ mass from body fat. Natural physiological human limits typically cap FFMI around 25.0 kg/m² for drug-free male athletes, providing a reliable diagnostic barrier that prevents heavily muscled individuals from being mislabeled as having excess adiposity.

Pediatric percentiles and the geriatric obesity paradox

Fixed adult BMI thresholds are clinically invalid at both ends of the human chronological lifespan: during childhood and adolescence, and in advanced senior years.

For children and teenagers aged 2 to 19 years, absolute numbers cannot be used because body fat percentage and skeletal architecture change continuously as bones lengthen, hormonal surges occur during puberty, and boys and girls diverge in body composition. Instead, clinicians utilize BMI-for-Age Growth Charts developed by the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO), applying the statistical LMS curve method to express child BMI as an age- and sex-specific percentile:

• Underweight: Below the 5th percentile
• Healthy Weight: 5th percentile to less than the 85th percentile
• Overweight: 85th percentile to less than the 95th percentile
• Obesity: 95th percentile or greater (with severe obesity classified as ≥ 120% of the 95th percentile)

A 10-year-old boy with a BMI of 21.0 kg/m² would be classified in the normal range under adult criteria, but on a pediatric growth curve, 21.0 kg/m² places him above the 95th percentile, warranting proactive family lifestyle evaluation.

At the opposite end of the spectrum, older adults aged 65 and above experience what epidemiologists designate as the Geriatric Obesity Paradox. Large-scale prospective cohort studies and meta-analyses demonstrate that the BMI range associated with the lowest all-cause mortality shifts upward with age:

• In young and middle-aged adults (ages 20 to 55), lowest mortality clusters tightly between 20.0 and 24.9 kg/m².
• In seniors aged 65 and older, lowest all-cause mortality is observed between 25.0 and 28.5 kg/m²—a bracket technically categorized as "overweight" by standard WHO definitions.

This survival advantage is biologically coherent. Modest adipose reserves provide essential nutritional and metabolic buffering during acute medical crises, pneumonia, or major surgical interventions. Furthermore, maintaining a slightly higher body mass correlates with greater bone mineral density, providing mechanical protection that significantly reduces the catastrophic risk of osteoporotic femoral neck (hip) fractures following accidental falls.

Comprehensive metabolic diagnostic action plan: beyond the bathroom scale

To take charge of your long-term cardiovascular and metabolic vitality, you should view your BMI not as a definitive verdict, but as a preliminary triage indicator. Medical professionals recommend uniting your height-to-weight metrics with a comprehensive tripartite diagnostic framework:

Pillar 1: Anthropometric Triad

Pair your BMI calculation with a monthly waist-to-height ratio check. Ensure your waist circumference remains below half your height (WHtR < 0.50). If accessible, schedule an annual dual-energy X-ray absorptiometry (DEXA) scan or multi-frequency bioelectrical impedance analysis (BIA) to track genuine visceral fat volume and skeletal muscle mass trajectories rather than scale weight alone.

Pillar 2: Blood Biomarker Panel

Request an annual metabolic blood panel from your physician that includes the following high-yield cardiometabolic biomarkers:

• Fasting Plasma Glucose & Glycated Hemoglobin (HbA1c): Assesses 90-day glycemic control (optimal HbA1c < 5.6%).
• Fasting Serum Insulin & HOMA-IR: Calculate the Homeostatic Model Assessment of Insulin Resistance via [Fasting Glucose (mg/dL) × Fasting Insulin (µIU/mL)] ÷ 405. A score below 1.5 reflects robust cellular insulin sensitivity; scores above 2.5 indicate significant metabolic resistance regardless of scale weight.
• Apolipoprotein B (ApoB) & Triglyceride-to-HDL Ratio: ApoB quantifies the exact particle count of all atherogenic lipoproteins. A Triglyceride-to-HDL ratio below 2.0 (in mg/dL units) is a powerful clinical proxy for small, dense LDL particles and hepatic insulin sensitivity.
• High-Sensitivity C-Reactive Protein (hs-CRP): Measures systemic vascular inflammation. Values below 1.0 mg/L indicate low cardiovascular inflammatory risk.
• Liver Enzymes (ALT, AST, GGT): Evaluates early hepatic steatosis and intrahepatic fat accumulation before irreversible fibrosis occurs.

Pillar 3: Functional Physical Capacity

Metabolic tissue quality is directly reflected in physical performance. Include functional markers in your routine health checks:

• Isometric Grip Strength: Measured using a hydraulic hand dynamometer. Grip strength is a potent independent predictor of cardiovascular mortality and all-cause mortality across all age groups.
• Cardiorespiratory Fitness: Estimated VO2 max or a standardized 6-minute walking distance. Higher cardiorespiratory fitness profoundly attenuates the health hazards of elevated BMI.
• Resting Hemodynamic Blood Pressure: Target resting systolic pressure < 120 mmHg and diastolic < 80 mmHg.

Sustainable Nutritional & Training Periodization

When implementing changes based on your calculator results, avoid extreme, crash calorie deficits (such as cutting 1,000+ kcal/day), which trigger severe metabolic adaptation, downregulate thyroid hormones (triiodothyronine / T3), and cannibalize lean skeletal muscle tissue. Instead, aim for a conservative deficit of 300 to 500 kcal per day, prioritize daily dietary protein intake between 1.6 and 2.2 grams per kilogram of target lean body mass to preserve nitrogen balance, and engage in progressive resistance exercise at least three days per week to signal to your physiology that muscle tissue must be preserved while adipose stores are mobilized.